Diabetes Insipidus (1).pptx presentation

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1. Diabetes Insipidus Medical Surgical Nursing Dept. NURSING DEPARTMENT CONS KANO

2. Diabetes insipidus Definition: DI can be defined as the disorder of posterior lobe of pituitary gland that characterized with excessive passage of large amount of diluted urine ( > 3L/24hrs, <300mosm/kg ) due to the deficiency of antidiuretics hormones (vasopressin ) or resistance to ADH in the kidney. Types There are two major forms of DI central and nephrogenic diabetes insipidus

3. Central diabetes insipidus; this form of DI is characterized by decreased secretion of antidiuretics hormones (ADH), also known as arginine vasopressin (AVP) which give rise polyuria and polydipsia by diminishing person’s ability to concentrate urine . Nephrogenic diabetes insipidus; this is characterized by decrease in the ability to concentrate urine by the kidneys owing to the resistance of ADH action from default kidneys it can be observed chronic renal insufficiency. Other two forms are gestational and dispogenic diabetes insipidus. Both the two are caused by deficiency of ADH but the deficiencies do not result from defects in the neurohypophysis or kidneys.

4. Etiology Diabetes insipidus is usually an acquired disorder with central having different causes than does nephrogenic DI. In rare cases both the two can may be inherited Causes of central DI Idiopathic 30% Malignant or benign tumor of the brain or pituitary gland 25% Cranial surgery 20% Head trauma 16% Hereditary, Other causes are; hypoxic encephalopathy, cancer of the lungs, lymphoma, tuberculosis, SCD, and arterio venous malformation anorexia nervo sa.

5. Causes of nephrogenic DI Lithium toxicity Hereditary Hypercalcemia (serum Ca + >11mg/ dL can impaired the urinary coc. Ability) Renal diseases eg amyloidosis Hypokalemia Hyperglycemia (osmotic diuresis) Drugs eg amphotericin B, demeclocycline , ofloxacin

6. Pathophysiology Idiopathic central DI presumably develops when cells in the hypothalamus are damaged or destroyed, identification of antibodies against AVP secreting cells may increasingly the role of inflammatory process and autoimmunity in DI is being recognized and cases of lymphocytic hypophysitis this cause lymphocytic infiltration of the stalk an posterior pituitary and subsequent decrease AVP production. In other hand as a result of excessive lithium ingestion ( lithium toxicity ) or hypercalcemia may cause dysregulation of aquaporin system in principal cells of the collecting ducts responsible for water raise channels that expressed exclusively in the kidney and this may result in the impairment of the urinary concentration

7. Clinical manifestation Polyuria, polydipsia and nocturia are the predominant manifestation of DI Excessive fatigue Head ache Dry skin Hair loss Diminish libido Dehydration Fullness of the bladder, flank abdominal pain which radiate to the testes or genital area

8. Deferential diagnosis Hypercalcemia Histocytosis Hypokalemia Medullary cystic diseases Types 1 DM Sickle cells diseases

9. Diagnosis History taking Physical examination Laboratory investigation; In patients with clinical symptoms a lab. Test must be perform to confirmed the diagnosis. These includes; == Urinalysis: A 24hrs urine collection to determine the urinary volume, osmolarity and specific gravity == Plasma ADH level == Water depravation test == Urea and electrolytes (U&E) == ADH stimulating test == simultaneous plasma and urinary osmolarity Imaging studies eg CT scan, MRI etc

10. Medical Management Hormonal replacement eg pitressin (5-10 units IM/SC q8-12hrly), desmospressin (inj. 4mcg/mL or tablet 0.1-0.2mg) Antidiabetics, Sulfonylureas eg chlopropamides 100-250mg Anticonvulsants; certain antiepileptic drugs such as carbamazepine have proven helpful in DI by promoting the release of ADH Diuretics, Thiazide eg hydrochlorothiazide this may reduce flow to ADH-sensitive distal nephron and it may induce mild volume depletion and cause proximal salt and water retention. NSAIDs eg ibuprofen diclonfenec etc these agent is believed to inhibit prostaglandin synthesis which reduces the the delivery of solute to distal tubules reducing urine volume and increasing urine osmolarity Potassium-Sparing Diuretics eg Amiloride to reduce the risk of hypokalemia when combined with thiazide diuretic (Reduce the risk of hypokalemia when thiazide diuretics used)

11. Nursing Management Assess the level of fluid depletion Monitor input and out put Vital signs Ensure adequate fluid intake (salt and water in balance proportion) Check for fluid retention and hyponatremia as it happened during the initial treatment Teach the patient to treat vomiting or diarrhoea during travelling or anything that cause dehydration Reassure the patient

12. Nursing Diagnosis Deficient fluid volume related to polyuria and nocturia Ineffective sexual pattern related to loss of libido and sexual dysfunction Risk for imbalance electrolyte related to hypokalemia and hyponatremia during initial treatment

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